Evidence map›Paper›PMID 27351135›Full record

ArticleOncotarget2016

Long non-coding RNA NEAT1 promotes non-small cell lung cancer progression through regulation of miR-377-3p-E2F3 pathway.

Chengcao Sun, Shujun Li, Feng Zhang, Yongyong Xi, Liang Wang, Yongyi Bi, Dejia Li

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 180 papers, 6 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
180citing papers in PubMed, 6 pooled it
25.4field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

180 citing papers in PubMed, 6 syntheses or guidelines pooled it, 322 citations in OpenAlex.

  1. Pooled it
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  13. Unraveling the Predictive Value ofStem cells international · 2026
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  19. [Predictive Value of miRNAs Markers for Advanced Lung Squamous Cell Carcinoma].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2025
    Article
  20. Article

120 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 1 institution in 1 country.

Chengcao SunDepartment of Occupational and Environmental Health, School of Public Health, Wuhan University, Wuhan, P. R. China.
Shujun LiDepartment of Occupational and Environmental Health, School of Public Health, Wuhan University, Wuhan, P. R. China.
Feng ZhangDepartment of Occupational and Environmental Health, School of Public Health, Wuhan University, Wuhan, P. R. China.
Yongyong XiDepartment of Occupational and Environmental Health, School of Public Health, Wuhan University, Wuhan, P. R. China.
Liang WangDepartment of Occupational and Environmental Health, School of Public Health, Wuhan University, Wuhan, P. R. China.
Yongyi BiDepartment of Occupational and Environmental Health, School of Public Health, Wuhan University, Wuhan, P. R. China.
Dejia LiDepartment of Occupational and Environmental Health, School of Public Health, Wuhan University, Wuhan, P. R. China.
Wuhan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recently, the long non-coding RNA (lncRNA) NEAT1 has been identified as an oncogenic gene in multiple cancer types and elevated expression of NEAT1 was tightly linked to tumorigenesis and cancer progression. However, the molecular basis for this observation has not been characterized in progression of non-small cell lung cancer (NSCLC). In our studies, we identified NEAT1 was highly expressed in patients with NSCLC and was a novel regulator of NSCLC progression. Patients whose tumors had high NEAT1 expression had a shorter overall survival than patients whose tumors had low NEAT1 expression. Further, NEAT1 significantly accelerates NSCLC cell growth and metastasis in vitro and tumor growth in vivo. Additionally, by using bioinformatics study and RNA pull down combined with luciferase reporter assays, we demonstrated that NEAT1 functioned as a competing endogenous RNA (ceRNA) for hsa-miR-377-3p, antagonized its functions and led to the de-repression of its endogenous targets E2F3, which was a core oncogene in promoting NSCLC progression. Taken together, these observations imply that the NEAT1 modulated the expression of E2F3 gene by acting as a ceRNA, which may build up the missing link between the regulatory miRNA network and NSCLC progression.

Indexed as

A549 CellsAdultAgedAged, 80 and overAnimalsCarcinoma, Non-Small-Cell LungCell Line, TumorDisease ProgressionE2F3 Transcription FactorFemaleGene Expression Regulation, NeoplasticHumansLung NeoplasmsMaleMiceMice, Inbred BALB CE2F3 protein, humanE2F3 Transcription FactorMicroRNAsMIRN377 microRNA, humanNEAT1 long non-coding RNA, humanRNA, Long NoncodingE2F3hsa-miRNA-377-3p (miR-377-3p)long non-coding RNA NEAT1 (lncRNA NEAT1)non-small cell lung cancer (NSCLC)tumorigenesis

Identifiers

PMID27351135
PMCPMC5239515
OpenAlexW2420947713

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.